Commercially available parenteral fat emulsions contain linoleic acid (18:2w6) as the principal fatty acid. Linoleic acid is converted to gamma-linolenic acid (18:3w6) with the aid of the enzyme, delta-6-desaturase. Gamma-linolenic acid is relatively rare in the human diet. Gamma-linolenic acid is found in human milk and in some oils such as borage oil. The conversion of linoleic acid to gamma-linolenic acid is the rate limiting step in the preparation of arachidonic acid and the prostaglandins, prostacyclin, PGE.sub.2 and thromboxane. Synthesis of prostacyclin and PGE.sub.2 is very desirable because they have a range of cytoprotective, antiaggretory, bronchodilation, vasodilation and anti-inflammatory properties.
Under certain conditions delta-6-desaturase is slow, absent or non-functioning in mammals. If linoleic acid is the primary nutritional fatty acid source, elevated levels of linoleic acid and an associated deficit of gamma-linolenic acid and other prostaglandin precursors can result. For example, gamma-linolenic acid production in neonates is low. Viral infections, saturated fats, aging, cancer, low zinc levels, alcohol, diabetes, Sjogren's syndrome and scleroderma also decrease the synthesis of gamma-linolenic acid and prostaglandins.
Thus, there is a need for a parenteral nutritional composition that avoids the effects of a deficit in the presence or function of delta-6-desaturase and increases the rate of formation of desirable prostaglandins.